Hair Treatment
Human hair is a thermoset of cross-linked, .alpha.-helix protein, primarily keratin. Keratin is composed of a complex of polypeptide chains of high molecular weight. Protein sequencing analysis of whole hair fiber using acid hydrolysis has found traces of all the amino acids in human hair, but suggests that cystine, glutamic acid, serine, leucine, aspartic acid, arginine and threonine are among the amino acids of highest prevalence in hair..sup.1 The human hair shaft is comprised of three concentric layers identified as the cuticle, a thin, outer-most shell, the cortex, the main body of the hair, and the medulla, a thin, central core. The cuticle and cortex are responsible for the hair shaft's mechanical properties (in some hair the medulla is absent). The cuticle is composed of flattened, scale-like platelets of amphoras keratin. Its condition is responsible for the outward appearance of the hair, particularly feel and shine. The cortex forms and is composed of long keratinous spindle cells containing numerous macrofibrils of intermediate filament protein, held together by an intercellular matrix of beta-keratose. Each macrofibril contains 11 protofibrils in a helical structure. Each of the protofibrils is composed of three alpha-helices, the fundamental fibrous keratin.
 FNT .sup.1 Gillespie and Inglis, Total S-Carboxymethyl Keratin Extracted from Guinea Pig Hair by Standard Methods (1965).
Alpha-helical keratin maintains its coil-shaped secondary structure by the use of hydrogen bonding between adjacent turns of the coil and by ionic bonding or salt bridges which pair the amine bases, lysine and arginine to the carboxylic acids, aspartic acid and glutamic acid. The method described herein changes the charge on the carboxylic acids within keratin causing both the loss of hydrogen bonding properties and the cleavage of the salt bridges. Secondary to these events is the disassociation of some of the disulfide bridges, or cystine bonds from the helix structure itself which are a principle force in the maintenance of natural curl. With the loss of hydrogen and ionic bonding, the keratin is partially denatured. The shaft becomes less sensitive to external moisture and more sensitive to heat-induced curling. With the partial loss of secondary and tertiary structure involving disulfide bridges, naturally curly hair loses its wavyness.
Those amino acids which are affected by the electron protonation of weak carboxylic acids (aq) resulting from the protonation of glutamic acid and aspartic acid are marked below by an asterisk.
The Amino Acid Composition of Hair Follicle Proteins (residues per 1000 amino acid residues).sup.2 Amino Acid Residues Cys 160* Asp 52* Thr 59 Ser 97 Glu 127* Pro 52 Cit 0 Gly 50 Ala 54 Met 0 Ile 31 Leu 64 Tyr 30 Phe 43 Lys 24* His 12 Arg 71* Isopeptide Trace .sup.2 Gillespie and Inglis, 1965, total S-carboxymethyl keratin extracted from guinea pig hair by standard methods.
Hair can be divided into four conformational categories: (i) straight, (ii) wavy, (iii) curly, and (iv) kinky. The amount of curl is directly associated with two factors: the alignment and shape of the follicle in the epidermis (the more angulated the follicle the more curly) and the shape of the shaft itself Straight hair resembles a rod with a circular diameter; wavy hair shafts are compressed into an oval diameter; curly shafts are further compressed into an elongated ellipse and kinky hair shafts are flatter still. Hair shaft configurations are as follows:
 Straight Wavy Curly Kinky ##STR1## ##STR2## ##STR3## ##STR4##
The elastic behavior of most hair types when wet is due to the hydrogen bonding that occurs between adjacent coils of keratin's secondary .alpha.-helix structure..sup.3 Hair becomes straighter when wet because hydrogen bonds--connecting the amino group of one amino acid and the oxygen of the third amino acid beyond it--are easily broken in water. The polypeptide chain can then be pulled out of its compact helical shape into a more extended form. As the hair dries the hydrogen bonds reform and the chains contract into their normal length. A similar, reversible breaking of hydrogen bonds occurs when hair is subject to tension or heat, as demonstrated by heat curlers, heat wands and heat combs. Keeton et al. describe the rubberband-like hydrogen bonds of .alpha.-helix keratin coils..sup.4
 FNT .sup.3 Knowlton, John, Handbook of Cosmetic Science and Technology, Justine-Avon Pty, South Africa. Excerpted from the chapter, The Structure of Hair, Cosmetic Science & Technology On-Line contents page.
 FNT .sup.4 Keeton, W. T., Gould, J. L., Biological Science, 5th Ed., W.W. Norton, New York, 1993, p. 67.
To permanently alter the natural curl or straightness of human hair, a number of types of bonds must be cleaved, including salt bridges and disulfide bonds..sup.5 Disulfide bridges (cystine bridges) often serve to attach separate keratin strands or hold the strand within the surrounding matrix. Current permanent waving and straightening methods break disulfide bonds into free sulfhydryls and then re-establish new disulfide bonds in the desired configuration by reduction/oxidation of the hair shaft using various chemicals sequentially. This manipulation of sulfur (S) within cysteine is possible by alkalis, bisulfides and other chemicals because cystine's small, aliphatic side chains contain polar groups that ionize readily. Nevertheless, the process is harsh on the hair and potentially harmful to the skin.
 FNT .sup.5 Menefee, E., Relation of keratin structure to its mechanical behavior, Appl. Polymer Symposium, 18, 809-821.
Disulfide bridges are most predominant in the outermost layer of the shaft's cuticle, the epicuticle, with progressively less found in the cuticle's sublayers, the exocuticle and endocuticle. The epicuticle also contains more disulfide bonds than does the matrix of the cortex..sup.6
 FNT .sup.6 The amount of cysteine and sulfur in tissue determines its hardness--tortoise shells, hooves, and horns are examples of the strength derived from cysteine bridges when up to one amino acid in four is cysteine. Keeton, W T, Gould, J. L., Biological Science, 5th Ed., WW Norton, New York, 1993., p. 67. ##STR5##
Current Methods of Permanent Hair Waving and Relaxing. New mechanical structure is imposed on hair shafts on a semi-permanent basis by the use of several types of chemicals capable of cleaving and reforming disulfide bonds in a two step process (reduction and oxidation) that results in the temporary denaturing of hair protein..sup.7 Several formulation improvements and additives have been developed in an effort to reduce the harshness of these chemicals and maintain pliable hair properties. Current methods, however, remain dangerous to the skin and eyes. Direct contact can result in second- and third-degree chemical burns or even hair loss..sup.8 None of the known methods are recommended if the scalp or skin is sensitive, scaly, scratched, sore or tender, and unsatisfactory, sometimes harmful results occur if the directions are not carefully followed.
 FNT .sup.7 Biochemistry 2001: Introductory Biochemistry, Mount Allison University, Dr. A. Cockshutt (1997); Protein Function: Folding of Structural proteins: Course Outline and Lecture Notes, Winter Term 1997.
 FNT .sup.8 The A.M.A. Book of Skin and Hair Care, Schoen, L A, Ed., American Medical Association, J.B. Lippincott Company, NY, 1976. p. 116.
During the permanent wave or straightening process, the hair is reshaped into waves with appliances or pulled straight by combing with lotions containing reducing agents. After 10 to 20 minutes, the free sulfhydryl groups are reoxidized and the hair conditioned and set with the desired conformity. While in a reduced state, the sulfhydryls within the matrix and protofibrils slide past each other as the protein is temporarily denatured. Once reoxidized, however, they form new cystine bridges and maintain this bond for a period of weeks or months.
Most permanent hair-waving and straightening products marketed today use one of five types of chemicals: (1) thioglycolate-based products, (2) sulfite-bisulfite products, (3) sodium hydroxide (alkali) products.sup.9, (4) lithium hydroxide and (5) acetamide (formulated as a between-shampoos, aerosol styling aid). In (1)-(4), the chemical lotion is applied to clean, damp hair that has been set in curlers or pulled straight by combing action. After a carefully-measured period of time, the disulfide bonds are broken, the solution is rinsed off, and a second solution (often hydrogen peroxide or other oxidizing agent) is applied to neutralize the reaction. Thioglycolate wave creams and straighteners produce reversible changes in the chemical disulfide bonds of hair by generating free oxygen radicals for 10 to 20 minutes. Thioglycolate may induce breakage if the hair has been bleached, dyed, previously straightened or permed..sup.10 Concern about the teratogenicity of thioglycolate has recently caused the United States Department of Health and Human Services to post notice of a need to review their safety for human use..sup.11
 FNT .sup.9 The AMA Book of Skin and Hair Care, Idid, p. 116-119.
 FNT .sup.10 A.M.A. Book of Skin and Hair Care, pp. 118-119.
 FNT .sup.11 Department of Health and Human Services, Public Health Service, National Institute of Environmental Health Sciences, National Toxicology Program reported in the Federal Register: Apr. 21, 1997 (Vol. 62, Number 76), pp. 19348-19349 (Notices). As of this date, the DHHS has solicited comments regarding chemicals sodium thioglycolate (CAS367-51-1) for reproductive toxicity (noting high production and occupational and human exposure in hair care products).
Bisulfite wave creams and straighteners also produce reversible bond changes. Bisulfite is milder on skin and the chance of hair damage is lower, permitting these products for home use. In the straightening procedure, bisulfite lotion is applied to clean, damp hair which is then covered in a plastic turban for about 15 minutes. The hair is then combed for 15 to 20 minutes to produce the degree of straightness desired. The disulfide bonds are relinked into a new orientation by rinsing the hair with water and applying an alkaline stabilizer solution followed by a conditioner. Results from this method are similar to alkali straighteners and superior to thioglycolates.
Like other known methods, alkali lotions cannot be used on irritated or injured scalps. As new hair grows in, it alone should be exposed to the chemical straighteners, an often delicate and difficult procedure that avoids lotion contact with both the scalp and the previously treated hair. In this method sodium hydroxide lotion is applied to the hair and smoothed flat with finger pressure. A `normalizer` pre-shampoo rinse is then applied followed by a water rinse. The hair is then shampooed twice, conditioned and administered a setting/styling/wrapping lotion prior to styling and drying. Some brands also add a leave-in "perm strengthener" after shampooing.
The "no lye" method uses lithium hydroxide, also a human toxin, in combination with other ingredients as the relaxing agent. This method begins with a moisturization additive, followed by the lithium cream, a pre-shampoo normalizer, neutralizing shampoo and a revitalizing conditioner. The user is also cautioned against skin and scalp burns, possible hair loss and eye injury. The product is contraindicated for persons with damaged or chemically-treated hair and irritated scalp.
Acetamide (CH.sub.3 CONH.sub.2) is an organic, crystal compound in the urea and guanine series which has recently been formulated into a cosmetic spray-on, straightener styling aid for use between shampoos. Damp, clean hair is sprayed with the acetamide aerosol and blown dry with tension brushing. Acetamide is a known irritant to the eyes, nose, and throat and has shown low-to-moderate acute toxicity from oral exposure, including liver tumors, in animal studies (Group 2B, possible carcinogen, IARC classification).
Other methods of breaking disulfide bonds in hair employ high-heat appliances. In this method heat combs set at 300.degree. F. are pulled quickly through long hair, which instantly breaks disulfide bonds leaving the hair straight. This process can result in damaging hair permanently if the temperature and combing speed are not carefully managed..sup.12
 FNT .sup.12 Significant alteration occurs to hair at 140.degree. to 250.degree. F. Large-scale irreversible damage occurs above 300.degree. F. American Medical Association Book of Skin and Hair Care., p. 193.
U.S. Pat. No. 3,654,936 to Wajaroff describes the use of a keratin softener for straightening hair. In this method hair is treated with a reducing agent then straightened by the action of a "keratin softener" combined with swelling or penetration-promoting agents, while being straightened mechanically prior to the application of a fixation agent.
Other straightening methods include the use of humectants such as fatty acid lactylates and fatty acid glycolates to improve the hair's texture,.sup.13 and the use of dipropylene glycol monomethyl ether as a swelling and penetrating agent..sup.14
 FNT .sup.13 U.S. Pat. No. 4,424,820, "Hair Straightening Compositions Containing Fatty Acid Lactylates and Glycolates and their Method of Use", Cannell, D. et al., assigned to Redken Laboratories.
 FNT .sup.14 U.S. Pat. No. 4,859,459, "Method of Shaping Human Hair Using Dipropylene Glycol Monomethyl Ether", Greiche, J., et al., assigned to Wella Aktiengesellschaft, Germany.
Nail Hoof, and Hyperkeratosis Treatment
Mammalian nails and hooves and hyperkeratotic skin tissues such as callouses, corns and the surrounding mounds of warts are also high in keratin protein and can be denatured by the compositions of the invention. This denaturing of keratin leads to the softening of surface keratin and keratin debris, the buildup of nail tissue under the nail plate medically known as onychomycosis (OM), a localized infection of the nail or nail bed caused by pathogenic fungi. While prevalent in both finger and toe nails, it is primarily a disorder of the toenails occurring more often in older adults and constituting between 18% and 40% of all nail disorders. Also known as tinea unguium, OM is caused by microorganisms of the dermatophyte family, candida albicans and, rarely, the mold scopulariopsis brevicaulis. OM initially presents as a thickening and opacification of the nail plate edges. White patches may form where air pockets occur and various degrees of erosion, subungual hemorrhaging and other discoloration can result as the fungus advances. Total dystrophic OM, which is the most advanced and common form, causes the nail plate to become thickened with underlying keratin debris elevating the nail plate at a severe angle to the nail bed. Pain and difficulty in wearing foot apparel is often experienced.
Current Methods of Treatment
Because dermatophytes are invasive to the keratin nail tissue, nail fungal infections are one of the hardest forms of external infection to treat. While current treatments are somewhat effective, they have adverse side-effects, and are contra-indicated for patients taking certain drugs. Recently FDA-approved Terbinafine (Lamisil.RTM.) is now the generally-accepted drug of choice. It is a synthetic allylamine compound that inhibits the action of squalene expoxidase, a crucial enzyme in the formation of ergosterol, leading to membrane disruption and dermatophytic cell death. Oral terbinafine is generally well-tolerated with the most common adverse effects being nausea, abdominal pain and allergic skin reactions. Taste disturbance and hepatic toxicity have also been reported. Itraconzole (Sporanox.RTM.) is an alternative treatment which inhibits cytochrome P450 dependent synthesis of ergosterol. Reported side effects include headache, rhinitis, upper respiratory tract infection, sinusitis, reversible hepatitis, severe hepatotoxicity, diarrhea, dyspepsia, flatulence, dizziness, nausea, cystitis, urinary tract infection, myalgia, appetite increase, constipation, gastritis, gastroenteritis, myalgia, fever, pain, tremor, herpes zoster, asthenia, pharyngitis, rash and vomiting. Numerous drug interactions with itraconzole also cause plasma level increases and decreases. Clinical trials indicate that 89% of users noted improvement, 14% were cured and 21% of the cured group experienced reinfection. In the past, griseofilvin, an antifungal agent derived from a number of penicillium species inhibiting cell division and nucleic acid synthesis, ketoconazole, an oral or topical synthetic ioxolane imidazole compound which interferes with the biosynthesis of ergosterol, and fluconazol, an oral synthetic bis-triazole compound that inhibits the cytochrome P450-dependent 14 alpha-demethylation step in the formation of ergosterol, were prescribed for OM and, for some patients, remain the drug of choice, despite a higher risk of severe side effects.
Like oral methods, topical medications for OM require continuing treatment over many (i.e., 3-18) months. Removal of the nail by surgical means or by 40% urea cream may hasten the total duration of treatment. Fungicidal creams include myconazole nitrate, clotrimazole, 10% povidine iodine and 1% econozole nitrate.
Callouses and Corns
Callouses and corns form a protective thick pad on the stratum corneum layer of the skin in response to repeated irritation or rubbing. They can appear anywhere on the body but are generally found over a bony spot on the hands, feet and elbows. A corn is a thickened area of keratin that occurs on the feet, usually over the joints of the toes. Corns can become painful if the thickened skin transfers pressure to the underlying bone. Callouses and corns can be treated with salicylic acid, pumice stone or by excision.
Plantar Warts
Plantar warts are hyperkeratotic lesions usually on the plantar surface (sole of foot) or palms caused by the Human Papilloma Virus (HPV) which attacks the epidermal layers through direct contact. The glabrous skin of soles and palms can be preferentially involved in various disorders of keratinization due to the higher concentration of keratin at these sites. Failure to treat plantar warts can lead to their transmission, recurrences and pain. Although self-resolving, they can be treated by cryotherapy, surgically (curettage, electrodesiccation), with topical acids (salicylic acid, lactic acid or cathandrin) or immunologically. Keratin is also found in abnormally high concentration in the non-ridged skin of patients with the Dowling-Meara form of epidermolysis bullosa simplex, for which the invention is also a treatment. While the invention cannot disable the virus, it can reduce the size of the surrounding keratinous tissue which is the source of plantar wart pain.
Psoriasis and Ichthyosiform Dermatoses
Psoriasis is an inherited disorder of keratin formation in which control of normal epidermal cell turnover has been lost leading to the production of abnormal keratin scales and raised formations known as plaques. The turnover rate of psoriatic keratinocytes (from basal layers to stratum corneum shedding) is only 3-4 days as compared to the 26-28 normal cell cycle. Psoriasis is characterized by scaling papules, most often occurring on the elbows, knees, hands, feet and scalp. Lesions appear pinkish in color with silver-white scales, are sometimes pruritic, and can be debilitating psychologically. Acitretin (retinoid-Vitamin A-analog), calcipotriol, cyclosporin and tazarotene are chemicals used to treat psoriasis by modulating the cellular differentiation of the epidermis and slowing down the production of keratin. In extreme cases, cytotoxic drugs (Methotrexate) and DNA-binding drugs (Trimethylpsoralen plus UV light) are used to slow the rate of cell division. In 30% of cases psoriasis also affects the nails and is characterized by discoloration, small pits in a thickened nail plate and onycholysis (separation of the nail late from the bed).
Hereditary ichthyosiform dermatoses are also hyperkeratotic cells which form fish scale patterns most often on the buttocks, thighs, shins, arms and backs of patients and are symptomatically treated by hydrating agents.
Acne Vulgaris and Keratosis Pilaris
Acne is a common inflammatory disease of the facial and upper torso skin in which sebaceous glands become obstructed as a result of the interplay between several factors: keratin-related chemicals, the steroid hormone, dihydrotestosterone (DHT), sebum, free fatty acids broken down from sebum, and the bacteria propionibacterium acnes. In acne the epidermal lining of the pilosebaceous duct does not keratinize properly so the keratin is not shed and instead adheres together, along with the sebum and bacteria present in the duct, causing the gland to plug and form painful, swollen, comedo lesions, commonly referred to as blackheads (open comedo), whiteheads (closed comedo) and blemishes (papules and pustules). The large, distended pore structure allows propionibacterium acnes to proliferate in combination with the chemical components of sebum resulting in the development of red pimples which, if lacerated, can leave permanent scaring. Acne is treated with Retin-A and various antibiotics to inhibit bacterial lipase production causing sebum conversion into highly irritating fatty acids.
Keratosis Pilaris is a disorder in which keratinous cells of the epidermis form plugs that fill the openings of hair follicles to form small, pointed pimples, most commonly on the upper arms, thighs and buttocks, but sometimes on the face, especially in children. The condition usually resolves in warm weather and presents only cosmetic problems.
Age Lines
Aging skin is the result of UVA and UVB light damage, and biological decline in collagen production, resulting in the slowing of cell mitosis within the dermis. Methods to reverse the appearance of fine lines and surface blemishes and stimulate skin cell renewal include beta hydroxy acids (salicylic and citric acids), Retin-A (tretinoin) and various "peeling" agents which remove the outer epidermis including the keratinous stratum corneum and attack the lower dermal layer to stimulate new collagen production. Increase collagen production has the effect of reducing age lines in the epidermis.
Background of Weak Acids
Weak acids are acids which only feebly conduct electricity (low conductivity) and are only partially ionized in solution. The conductivity of solutions of acids has been thoroughly studied and the electrical conductivity of the weak acid, glacial or acetic acid (C.sub.2 H.sub.3 O.sub.2 H), for example, at a molarity of 0.1 is 4.67 reciprocal ohms (mho). This contrasts to the conductivity of strong acids which ionize completely in solution and have high conductivities ranging from 60 to 350 mho at the same molarity. Weak acids ionize only partially and their ions continue to react with each other, dissociating and recombining continuously in a condition known as the position of equilibrium. As is known, this occurs because the polar water molecules start to break the acids into its ions but cannot stop them from also being attracted to each other. While water molecules are sufficiently polar to prevent any permanent recombinations of the ions of strong acids, water is less effective at this task in handling weak acids and recombination of ions begins to take place as soon as any appreciable concentration of ions is present in the solution. Once the rate of recombination catches up to the rate of dissociation both processes continue to proceed at the same rate and a state of equilibrium then exists..sup.15
 FNT .sup.15 Hess, Fred C., Revised by Thomas, Arthur L., Chemistry Made Simple, Rev. Ed 1984, Doubleday & Co, NY 1984, p. 71-74.
It is further known that if 0.01 mole of pure acetic acid is dissolved in a liter of water at room temperature, about 4% of the solute will be ionized by the time equilibrium is reached. However, this position of equilibrium will vary depending upon the temperature and concentration. For example, if 0.1 mol of pure acetic acid is added to a flask so that the final volume is 1 liter, only 1.3% of the acetic acid is ionized to acetates..sup.16 The remaining 98.7% remains in solution. The higher the percentage of weak acid, the stronger the denaturing properties of the solution by protonation of keratin's carboxylic amino acids. An increase in temperature will also shift the position of equilibrium in the direction of the process absorbing energy and make the acid more reactive with carboxylic amino acids. Thus the reactivity of the solution can be modulated by both the concentration of the solution and its temperature.
 FNT .sup.16 Organic Chemistry, Ibid., p. 772.
Acetic acid (CH.sub.3 COOH) is a non-polar solvent (Subclass 102): ##STR6##
Acetic acid is identified as glacial acetic acid (in pure form), and in water solution as ethanoic acid, ethylic acid, methanecarboxylic acid, pyroligeneous acid, and vinegar acid.
For example, vinegar, a 5% aqueous solution of acetic acid, is produced by fermentation of sugars and starches. In fact, when fermented alcoholic beverages such as wine and cider are exposed to the air, the alcohol is converted to acetic acid.
Acetic acid is used in the manufacture of acetic anhydride, cellulose acetate, vinyl acetate monomer, acetic esters, chloroacetic acid, as well as the production of plastics, pharmaceuticals, dyes, insecticides, photographic chemicals, etc.; it is also a food additive (acidulant), a latex coagulant, oil-well acidizer and is used in textile printing..sup.18 Acetic acid is recognized in the art as a fixing agent of protein capable of preserving both the structure and/or chemical composition of animal or plant tissues without combining with or precipitating any proteins..sup.19 Acidic acid solutions for the purification of proteins include methods to purify fragments of fibrinogen important to blood-clotting..sup.20 It is also known in the practice of biochemistry peptide sequencing that disulfide bonds can be oxidized in vitro by the carboxylic acid, performic acid,.sup.21 which converts all cys residues--whether linked by disulfide bridges or not--to cysteic acid residues that are stable in both acidic and basic solutions. The vulnerability of disulfide bonds to acetic acid attack has also been utilized in foodstuff processing.sup.22 and cheese manufacture.
 FNT .sup.18 Hawley, Gessner G., The Condensed Chemical Dictionary, 9th Ed., Van Nostrand Reinhold Co, New York, 1977, p. 5.
 FNT .sup.19 Four types of fixing agents are possible: (1) Additive, coagulant, (2) additive, non-coagulant, (3) non-additive, coagulant, and (4) non-additive, non-coagulant. Other major fixing agents defined by category are: Acetone (3), chromium trioxide (1), ethanol (3), formaldehyde (2), glutaraldehyde (2), mercuric chloride (1), methanol (3), osmium tetroxide (2), picric acid (1), potassium dichromate (2) and trichloracetic acid (3).
 FNT .sup.20 The Euglobulin Clot Lysis time test (CPT code: 85360) uses 10% acidic acid solution to precipitate fibrinogen prior to mixing it with thrombin to measure clot lysis time.
 FNT .sup.21 Source: Biochemistry 659: Class Notes, Perdue University, 1967.
 FNT .sup.22 Keck-Gassenmeier B., Wieser H. (1996), Disulfide bonds in acetic acid: Soluble and insoluble glutenin fractions. In: Gluten '96, Proceedings of the 6th International Gluten Workshop (Wrigley C. W., ed.) RACI, North Melbourne, Australia, pp. 145-148.
Previous Uses of Acetic Acid on Hair
U.S. Pat. No. 5,635,168 to Burns et al. describes a composition and a method which claims to eliminate the rinsing step between reduction and oxidation, improving feel, curl retention, color receptivity and retention, shine, and strength of the hair, and is said to prevent or repair hair damaged by chemical waving or colorants. The compositions contain, (i) a polyvalent metal compound selected from alkaline earth metals (preferably a water-soluble salt such as magnesium sulfate), zinc compounds, and aluminum compounds; (ii) low molecular weight sulfur-containing material that can form disulfide bonds involving the keratin of hair (e.g., cystine-containing materials such as polypeptide or other proteinaceous materials), and (iii) optionally, an acid, which can be a carboxylic acid (e.g., a hydroxycarboxylic acid such as citric acid) or other organic acid (e.g., acetic acid) or mineral acid, wherein the pH of the compositions is less than 10. The compositions are said to be useful for the prevention or repair of damaged hair when applied in a process involving waving (after a waving solution has been applied to the hair and before an oxidizing agent has been applied to the hair).
U.S. Pat. No. 4,030,512 to Gaetani, et al. (entitled "Hair Lacquer or Setting Lotion containing Bi- or Tri-sequenced Copolymer"), describes a hair lacquer/hair setting lotion composition in a solvent comprising 0.2 to 10% by weight of a bi- or tri-sequenced copolymer. The copolymer comprises at least one sequence of a saturated hydrocarbon chain containing 2-4 carbon atoms, or a hydrocarbon chain containing 2-4 carbon atoms and interrupted by sulfur or oxygen. In the formula of Gaetani, R.sup.1 and R.sup.2 are alkyl C.sub.1-4, n is 0 or 1, and HX is hydrochloric, hydrobromic, lactic or acetic acid, and at least one sequence resulting from the anionic polymerization of a polymerizable monomer." Although acetic acid is mentioned, the composition in Gaetani is used as a temporary setting lotion that does not claim to physically alter the hair permanently. The process involves applying to the hair an effective amount of the composition, rolling the hair on rollers and applying external heat to the hair for a period of time ranging from 3 to 20 minutes.
U.S. Pat. No. 4,240,450 to Grollier, el al., describes the compositions having a combination of an anionic polymer and a cationic copolymer containing sulfonic acid, carboxylic acid or a phosphoric acid end unit, wherein the compositions are said to be useful for treating keratin materials.
Traditional and home recipes describe the use of vinegar (acetic acid) or lemon juice (citric acid) to clean hair and enhance its shine. Vinegar is recommended by the American Medical Association as an after-shampoo rinse if soap and hard water are used to clean hair. Vinegar rinse is said to remove the "scum" formed on hair shafts by the reaction of hard water minerals and salts with soap..sup.23
 FNT .sup.23 American Medical Association Book of Skin and Hair Care, Schoen, L A, Ed., J.B. Lippencott Co., New York, 1976, p. 26.